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. 2021 Nov 16;41(4):550–559. doi: 10.1038/s41388-021-02088-7

Fig. 7. Mitochondrial ROS plays an important role in the combined effect of ODN and oxaliplatin, via the CK2/OTUB1/p53/Bax signaling pathway.

Fig. 7

A–C Caki-1 cells were pretreated for 30 min with an ROS scavenger (NAC, GEE, or Trolox) (A), a NOX inhibitor (apocynin) (B), or a mitochondrial ROS inhibitor (Mito-TEMPO or MnTMPyp) (C), and then treated with 2 μM ODN for 24 h. D Caki-1 cells were pretreated with a Mito-TEMPO, MnTMPyp, DPI or apocynin for 30 min, and then treated with a combination of 2 μM ODN and 25 μM oxaliplatin for 24 h. E Caki-1 cells were pretreated with CK2 inhibitors (emodin and DRB) for 30 min, and then treated with 2 μM ODN for 3 h. F Caki-1 cells were transfected with control siRNA or CK2 siRNA, and treated with 2 μM ODN for 3 h. Mitochondrial ROS production was analyzed by fluorescence microscope or flow cytometry using MitoSOX Red. Protein expression and apoptosis were measured by western blotting (A–D) and flow cytometry (E, F). The values in the graphs D–F represent the mean ± SD of three independent experiments. *P < 0.01 compared to the ODN-plus-oxaliplatin treatment.